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Ninzima, S.

Publications and source records attributed to Ninzima, S..

2 recordsLinked to original sources

Lysine-rich regions located in the C-terminal domain of DNA Topoisomerase 2-alpha act as polyphosphoinositide interaction sites and nucleolar localisation signals

Polyphosphoinositides (PPIn) are lipid signalling molecules that regulate essential cellular processes in eukaryotic cells by regulating effector proteins not only in the cytoplasm, but also in the nucleus. To decipher PPIn nuclear functions, we have previously established quantitative proteomic methods in combination with PPIn pull-down to identify nuclear PPIn-binding proteins. We focused our analyses on one of these proteins, DNA Topoisomerase 2 (TOP2A), an enzyme known to resolve DNA topological problems occurring during replication, transcription and mitosis. In this study, we validated its direct interaction with PPIn and identified the binding site consisting of two lysine-rich polybasic regions (PBR) located within its C-terminal domain (CTD) at residues 1228-1237 and 1259-1276. Overexpression studies of the WT and PBR deletion mutants showed that these two PBR were required for TOP2A nucleolar localisation. TOP2A is localised to different sub-nuclear sites where PPIn have also been detected. We hence investigated the localisation of TOP2A by immunofluorescence microscopy and cell fractionation in relation to PPIn. We show that TOP2A colocalised with the PPIn phosphatidylinositol(4,5)bisphosphate (PtdIns(4,5)P2) in nuclear speckles of transcriptionally arrested HeLa cells. Inhibition of type II phosphatidylinositol-5-phosphate 4-kinase, which generates PtdIns(4,5)P2 from PtdIns5P, led to an increase of TOP2A levels associated with the chromatin. Our results demonstrated TOP2A as a PPIn effector protein and a role for nuclear PPIn in regulating the subnuclear dynamic of TOP2A.

molecular biology↗

TGF-beta promotes microtube formation in glioblastoma through Thrombospondin 1

Microtubes (MTs), cytoplasmic extensions of glioma cells, are important cell communication structures promoting invasion and treatment resistance through network formation. MTs are abundant in chemoresistant gliomas, in particular glioblastomas (GBMs), while they are uncommon in chemosensitive IDH-mutant and 1p/19q co-deleted oligodendrogliomas. To identify potential signaling pathways involved in MT formation we performed a bioinformatics analysis of TCGA data showing that the TGF-{beta} pathway is highly activated in GBMs compared to oligodendroglial tumors. In particular we observed that signaling pathways involved in extracellular matrix organization are differentially expressed between these tumor entities. Using patient-derived GBM stem cell lines, we demonstrated that TGF-{beta}1 stimulation promotes enhanced MT formation and communication via Calcium signaling. Inhibition of the TGF-{beta} pathway significantly reduced MT formation and its associated invasion in vitro and in vivo. Downstream of TGF-{beta}, we identified thrombospondin 1 (TSP1) as a potential mediator of MT formation in GBM through SMAD activation. TSP1 was upregulated upon TGF-{beta} stimulation and enhanced MT formation, which was inhibited by TSP1 shRNAs in vitro and in vivo. In conclusion, TGF-{beta} and its downstream mediator TSP1 are important mediators of the MT network in GBM and blocking this pathway could potentially help to break the complex MT driven invasion/ resistance network.

cancer biology↗